The epithelial sodium channel (ENaC) consists of three subunits (a-, b- and g-) and gain-of-function mutations in these genes cause hypertension in humans. ENaC in the brain may be activating central mechanisms contributing to salt sensitive hypertension. In the present study, we assessed expression of ENaC in the brain and kidneys. By RT-PCR, the a-, b- and g- subunits of ENaC were found in rat brain and the DNA sequences of the three subunits in the brain and kidney were identical. By real-time quantitative RT-PCR, the level of expression of the ENaC subunits was ~100 fold less in the hypothalamus compared to the kidney. The mRNA abundance ratio of the a-, b- and g-subunit was 20:1:1 in the brain, clearly different from the 5:1:1 ratio in the kidney. There were no significant differences in the level of the three subunit transcripts in the hypothalamus of 5 week-old Dahl S and R rats on regular salt intake, neither after high (1370 µmol Na⁺/g) vs regular (120 µmol Na⁺/g) salt diet for 2 weeks. However, a-ENaC subunit transcript abundance was reduced by ~30% (p<0.05) in the kidney of Dahl rats on high vs regular salt diet. Two weeks i.c.v infusion of aldosterone did not alter ENaC mRNA levels in the hypothalamus of Wistar rats. These results indicate that rat brain expresses ENaC subunits that are similar to those in the kidney but the level of their expression as well as their regulation in response to dietary salt and aldosterone appear quite distinct.